A hypoglycemic infant with secondary occipital brain injury defined by serial computed tomography and magnetic resonance imaging is described. An additional 22 similar cases were previously published in the English language literature. A total of 23 cases (including the present case) were reviewed. Abnormal brain imaging findings are associated with profound hypoglycemia and show involvement of the occipital lobes in 82% of affected newborns. Half of these infants had visual impairment, and their median and range of plasma glucose values, and postnatal age when hypoglycemia was first detected, were 7 mg/dL (range, 2-26 mg/dL) and 48 hours (range, 1-72 hours), respectively.
Apparently "stable" anemic premature infants may be in a clinically unrecognized high cardiac output state, and some echocardiographic measurements do not improve within 48 hours after transfusion. The benefits of transfusion practices guided by measures of cardiac function should be evaluated.
There is extreme variation in the definition of low plasma glucose levels in newborn infants in the first postnatal days, ranging from < 30 to < or = 60 mg/dL. The goal of the present study was to define low thresholds (< or = 5th percentile) of plasma glucose concentrations in full-term normal newborns during the first 72 hours of life. Population meta-analysis was performed on published studies of neonatal hypoglycemia ascertained by MedLine search. One-way analysis of variance was computed across the studies for each of the following four postnatal time periods: 1 to 2 (physiological nadir), 3 to 23, 24 to 47, and 48 to 72 hours. The estimated < or = 5th percentiles of neonatal hypoglycemia during 1 to 2, 3 to 23, 24 to 47, and 48 to 72 hours after birth were < or = 28, < or = 40, < or = 41, and < or = 48 mg/dL, respectively. Based on this statistical definition, we recommend that low thresholds of plasma glucose levels of 28, 40, and 48 mg/dL be adopted in full-term normal newborns at 1 to 2, 3 to 47, and 48 to 72 hours of life, respectively.
Results of a national survey of the current use of steroids in newborns in 1993 showed that 95% of the neonatologists in the United States have used dexamethasone for neonates at risk for chronic lung disease. Dexamethasone therapy for a period of a week or longer is associated with suppression of the hypothalamic-pituitary-adrenal axis (HPAA) in a substantial number of premature infants. A review of our current understanding of the biochemical tests evaluating HPAA function in premature infants and suggested guidelines for HPAA evaluation and management following dexamethasone therapy are presented.
Increased risk of central venous line thrombosis in tiny premature infants occurs because the size of the catheter relative to the cross-sectional area of the vessel is large, decreased plasma levels of plasminogen and antithrombin III, and relative low flow of the infusate through the catheter, in comparison with larger infants. A potentially fatal complication of central venous catheters is an intracardiac thrombus. The yield of detecting right atrial thrombi by routine echocardiographic monitoring is very low. Persistent positive blood cultures in infants with central venous lines, in spite of appropriate antibiotic therapy, or signs of catheter occlusion, may increase the yield of echocardiographic detection of intracardiac thrombi. Surgical removal of intracardiac thrombi in infants weighing less than 1500 gm carries a high mortality rate because of the need to use cardiopulmonary bypass with total circulatory arrest and profound hypothermia during surgery. It is in these infants that thrombolysis with urokinase should be considered. A successful therapy with urokinase of a complete occlusion of the right pulmonary artery by an embolus originating from the right atrium is described in a premature infant. For thrombolysis, a loading dose of urokinase of 4400 U/kg followed by 4400 to 8800 U/kg/hr for a few days was used. The thrombolytic effect was manifested by decreased thrombus echogenicity followed by its disappearance, by increased fibrinogen split products, and by decreased plasma fibrinogen. Urokinase therapy may cause massive bleeding, dislodge an intracardiac thrombus causing obstruction of cardiac valves or main vessels or causing embolization to the pulmonary or systemic circulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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